Tesi: "Nitric oxide"

1

Davies, Nathan Alun. "Nitric oxide in sepsis". Thesis, University of Essex, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285823.

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2

Molinari, Micol Ariella. "Nitric oxide synthase and the contribution of nitric oxide to vertebrate motor contol /". St Andrews, 2008. http://hdl.handle.net/10023/489.

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3

Illes, Mary. "Role of nitric oxide and nitric oxide synthases in the rice blast fungus". Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670065.

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4

Petersson, Joel. "Nitrate, Nitrite and Nitric Oxide in Gastric Mucosal Defense". Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8624.

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The human stomach normally contains high levels of bioactive nitric oxide (NO). This NO derives from salivary nitrate (NO₃^-) that is converted to nitrite (NO₂^-) by oral bacteria and thereafter non-enzymatically reduced in the acidic gastric lumen to NO. Nitrate is a common component in vegetables, and after ingestion it is absorbed in the small intestine. Interestingly, circulating nitrate is then concentrated by the salivary glands. Hence, intake of nitrate-rich vegetables results in high levels of NO in the stomach. The physiological effects of the high concentration of NO gas normally present in the gastric lumen have been hitherto unknown, and the present investigations were therefore conducted to address this issue.

NO produced in the gastric lumen after nitrate ingestion increased gastric mucosal blood flow and the thickness of the firmly adherent mucus layer in the stomach. The blood flow and mucus layer are essential defense mechanisms that protect the mucosa from luminal acid and noxious agents. Nonsteroidal antiinflammatory drugs (NSAID) are commonly prescribed and effective drugs for treating pain and inflammation, but are associated with severe gastrointestinal side effects. We demonstrated that a nitrate-rich diet protects against NSAID-induced gastric damage, as a result of the increased formation of NO in the stomach. We also showed that the gastroprotective effect attributed to nitrate depended completely on conversion of nitrate to nitrite by the bacterial flora colonizing the tongue, and that the oral microflora is therefore important in regulating physiological conditions in the stomach.

In summary, this thesis challenges the current dogma that nitrate intake is hazardous, and on the contrary suggests that dietary nitrate plays a direct role in regulating gastric homeostasis. It is likely that a sufficient supply of nitrate in the diet together with the oral microflora is essential for preventing pathological conditions in the gastrointestinal tract.

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5

Madrasi, Kumpal J. "Preservation of Nitric Oxide Availability as Nitrite and Nitrosothiols". FIU Digital Commons, 2012. http://digitalcommons.fiu.edu/etd/805.

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Nitric Oxide (NO) has been known for long to regulate vessel tone. However, the close proximity of the site of NO production to “sinks” of NO such as hemoglobin (Hb) in blood suggest that blood will scavenge most of the NO produced. Therefore, it is unclear how NO is able to play its physiological roles. The current study deals with means by which this could be understood. Towards studying the role of nitrosothiols and nitrite in preserving NO availability, a study of the kinetics of glutathione (GSH) nitrosation by NO donors in aerated buffered solutions was undertaken first. Results suggest an increase in the rate of the corresponding nitrosothiol (GSNO) formation with an increase in GSH with a half-maximum constant EC50 that depends on NO concentration, thus indicating a significant contribution of ∙NO2 mediated nitrosation in the production of GSNO. Next, the ability of nitrite to be reduced to NO in the smooth muscle cells was evaluated. The NO formed was inhibited by sGC inhibitors and accelerated by activators and was independent of O2 concentration. Nitrite transport mechanisms and effects of exogenous nitrate on transport and reduction of nitrite were examined. The results showed that sGC can mediate nitrite reduction to NO and nitrite is transported across the smooth muscle cell membrane via anion channels, both of which can be attenuated by nitrate. Finally, a 2 – D axisymmetric diffusion model was constructed to test the accumulation of NO in the smooth muscle layer from reduction of nitrite. It was observed that at the end of the simulation period with physiological concentrations of nitrite in the smooth muscle cells (SMC), a low sustained NO generated from nitrite reduction could maintain significant sGC activity and might affect vessel tone. The major nitrosating mechanism in the circulation at reduced O2 levels was found to be anaerobic and a Cu+ dependent GSNO reduction activity was found to deliver minor amounts of NO from physiological GSNO levels in the tissue.

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6

Liu, Jia Clinical School Prince of Wales Hospital Faculty of Medicine UNSW. "Nitric oxide in airway inflammation". Publisher:University of New South Wales. Clinical School - Prince of Wales Hospital, 2009. http://handle.unsw.edu.au/1959.4/43678.

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Exhaled breath condensate (EBC) is a non-invasive method of investigating airway inflammation associated with nitric oxide (NO) and the metabolites nitrite/nitrates (NOx) in diseases such as chronic obstructive pulmonary disease (COPD), but some of the variables affecting the results are unknown. It was hypothesised that 1) EBC would be influenced by lung volumes and the type of EBC collection device; 2) fractional exhaled NO (FENO) and EBC NOx in COPD patients would be altered by smoking and glucocorticosteroids (GCS); 3) cigarette smoke could contribute to the EBC NOx concentration while it may also decrease FENO indirectly by converting airway NO to NOx. It was found that EBC volume was significantly correlated with both tidal volume and minute volume. Comparing four EBC collection devices demonstrated greater efficiency with the ECoScreen?? than siliconised glass tubes or RTube?? but it gave factitiously high NOx levels. Total EBC protein levels over a 10-minute collection were significantly higher using the ECoScreen?? than either glass or RTube?? devices. A cross-sectional study of 96 COPD patients and 80 age-matched control subjects demonstrated that FENO levels in COPD patients were significantly higher than normal subjects when comparing either the combined groups or appropriate two subgroups: ex-smokers and smokers. GCS treatment demonstrated no significant effect on either FENO levels or EBC NOx, but EBC NOx was elevated in smokers. In vitro, cigarette smoke extract (CSE) induced significantly higher NOx and asymmetric dimethylarginine (ADMA) levels in A549 cells when compared with control media. The anti-oxidant, NAC pre-treatment partially reversed the elevated NOx levels but not the ADMA levels. This thesis is the first to report FENO and EBC NOx in COPD patients in an appropriate sample size to be able to evaluate each subgroup, and the increased EBC NOx levels found in smokers in vivo was consistent with the elevated NOx level in response to CSE observed in vitro. These data indicate that smoking-related airway inflammation and activation of the NO pathway are complex with both an increase in ADMA, NO, NOx and may be regulated by oxidative stress rather than the nitric oxide synthase (NOS) pathway.

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7

Bescós, García Raúl. "The effect of nitric oxide donors on human performance". Doctoral thesis, Universitat de Barcelona, 2011. http://hdl.handle.net/10803/62896.

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Nitric oxide or nitrogen monoxide (NO) is a tiny free radical gas. The discovery of this intriguing molecule has revolutionized physiology and pharmacology research during the last 20 years. Currently, it is known that NO is endogenously synthesized by several molecules and tissues via two pathways: the synthase-dependent pathway and the synthase-independent pathway. In the first, the amino acid L-arginine is the main donnor of NO synthesis. In the second, inorganic nitrate is the main substrate for the synthesis of this molecule. Interestingly, both pathways are directly connected. While the synthase-dependent pathway is oxygen dependent, the synthase-independent metabolic route is greatly facilitated under hypoxia conditions. Thus, these mechanisms of NO production regulate levels of NO in the tissues. An adequate production of NO is important because it plays an essential role in mechanisms related with vasodilatation and blood flow distribution. Additionally, NO modulates other important functions in the human body such as mitochondrial respiration and immune mechanisms. For all these reasons, the interest for dietary NO donors have increased during the last years. It has been suggested that the consumption of food rich in L-arginine or in inorganic nitrate may enhance NO availability in the human body. This hypothesis has not been unnoticed in exercise physiology. In fact, it has been suggested that supplementation with NO donors may improve the cardio-respiratory response, as well as the tolerance to endurance exercise in humans. However, there is a lack of studies analyzing this issue. Therefore, the aim of this doctoral thesis was to assess the effect of L-arginine and inorganic nitrate in the cardio-respiratory and metabolic response of healthy humans. To develop this aim, three studies and one review were carried out. In the first, it was found that L-arginine supplementation during three days at several doses, between 5.5 and 20.5 g/day was not effective to increase plasma markers of NO, as well as the cardio-respiratory and metabolic response during endurance test. In the second study we found that acute dose of inorganic nitrate supplementation (10 mg/kg of body mass) raised significantly plasma levels of nitrate and nitrite. However, this effect did not report an improvement in the cardio-respiratory response at low-to-moderate intensities of exercise. However, at maximal work loads of exercise dietary nitrate induced significantly reduction of oxygen consumption (VO2peak) compared with placebo. Other cardio-respiratory parameters, as well as blood lactate concentration did not differ between nitrate and placebo. In addition, exercise performance measured as time to exhaustion during an incremental test did not increase compared with placebo. All these findings together suggested that at higher intensities of exercise energy production became more efficient after inorganic nitrate ingestion. Accordingly, in the third study it was analyzed the effect of dietary inorganic nitrate ingestion for three days during endurance exercise in a cycle ergometer at high intensity (time-trial of 40-min). Results of this study showed that nitrate supplementation did not increase significantly plasma levels of nitrite, as well as enhance performance in healthy subjects. Interestingly, a significant, negative correlation was found between change in nitrite and endurance capacity measured as VO2peak during the exercise test. These results indicated that the effect of dietary nitrate ingestion was lower in subjects with high cardiovascular capacity compared with subjects with poor tolerance capacity to endurance exercise. This fact is very important, since it is known that endurance training increase values of VO2peak in sedentary population and this fact is correlated with lower incidence of cardiovascular diseases. These and other important conclusions of these studies are included in the last work of this thesis which was a review article.
L’òxid nítric (NO) es un radical lliure alliberat per diverses molècules i teixits en l’organisme humà. El descobriment d’aquesta intrigant molècula ha revolucionat la recerca en el camp de la fisiologia i la farmacologia durant els últims 20 anys. Actualment, es coneix que la alliberació de NO per part de les cèl•lules endotelials estimula el procés de vasodilatació. A més, també es coneix que aquesta molècula es un important regulador de la respiració mitocondrial i del sistema immunològic. Totes aquestes funcions han generat un gran interès per els precursors nutricionals de NO. En l’àmbit de la fisiologia de l’exercici físic s’ha suggerit que la suplementació amb alguna d’aquestes substancies (L-arginina o nitrat inorgànic) pot millorar la tolerància a l’exercici físic de resistència. No obstant, hi ha molta controvèrsia en els resultats dels estudis que han analitzat aquesta hipòtesi. Per tant, l’objectiu principal d’aquesta tesi doctoral va ser analitzar els efectes dels principals precursors de NO, L-arginina i nitrat inorgànic, en la resposta cardiorrespiratòria i metabòlica durant l’exercici físic de caràcter aeròbic en humans. Per dur a terme aquest objectiu es van realitzar 3 estudis i una revisió bibliogràfica. Els principals resultats d’aquests estudis van mostrar que la suplementació de L-arginina en diferents dosis no va ser efectiva per augmentar el marcadors plasmàtics de NO, així com, la resposta cardiorrespiratòria i metabòlica durant un exercici físic aeròbic en intensitats moderades. En referència als nitrat inorgànic, es va observar que la suplementació augmenta els nivells d’aquests compostos en plasma. No obstant, aquest fet no es va correlacionar amb una millora de la tolerància a l’exercici físic de resistència. A més, es va observar una correlación negativa i significativa entre l’augment dels nitrits plasmàtics i la potència aeròbica màxima (VO2max). Tots aquests resultats van ser àmpliament tractats en l’últim treball (revisió bibliogràfica) d’aquesta tesi. En resum, l’ingesta nutricional de L-arginina i/o nitrat inorgànic no resulta efectiva per millorar la resposta cardiorrespiratòria i la tolerància a l’exercici físic de resistència en humans sans i entrenats físicament.

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8

Murrell, George Anthony Calvert St George Clinical School UNSW. "Nitric oxide and tendon healing". Awarded by:University of New South Wales. St George Clinical School, 2006. http://handle.unsw.edu.au/1959.4/31887.

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Nitric oxide is a small free radical generated by family of enzymes, the nitric oxide synthases. In a series of experiments performed over the last 15 years we showed that nitric oxide is induced by all three isoforms of nitric oxide synthase during tendon healing and that it plays a crucial beneficial role in restoring tendon function. In normal tendon we found very little nitric oxide synthase activity while in injured rat and human tendons nitric oxide synthase activity was expressed in healing fibroblasts in a temporal fashion. In healing rat Achilles tendon fibroblasts the first isoform to be expressed was endothelial nitric oxide synthase (eNOS), followed by inducible nitric oxide synthase (iNOS), and then brain or neuronal nitric oxide synthase (bNOS). Systemic inhibition of nitric oxide synthase activity decreased the cross sectional area and mechanical properties of the healing rodent Achilles tendons. Addition of nitric oxide via NO-flurbiprofen or NO-paracetamol enhanced rat Achilles tendon healing. Addition of nitric oxide to cultured human tendon cells via chemical means and via adenoviral transfection enhanced collagen synthesis, suggesting that one mechanism for the beneficial of nitric oxide on tendon healing might be via matrix synthesis. The final part of the work involved three randomized, double-blind clinical trials which evaluated the efficacy of nitric oxide donation via a patch in the management of the tendinopathy. In all three clinical trials there was a significant positive beneficial effect of nitric oxide donation to the clinical symptoms and function of patients with Achilles tendinopathy, tennis elbow and Achilles tendonitis.

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9

Gahm, Caroline. "Nitric oxide in brain contusion /". Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-392-2/.

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10

Ashley, Euan A. "Nitric oxide and cardiac function". Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249192.

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11

Musialek, Piotr. "Nitric oxide and cardiac pacemaking". Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326119.

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12

McKinlay, Alistair C. "New nitric oxide releasing materials". Thesis, University of St Andrews, 2010. http://hdl.handle.net/10023/932.

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The aim of this thesis was to examine the ability of metal organic frameworks (MOFs) to store and controllably release biologically significant amounts of nitric oxide (NO). Initial work involved the synthesis of a series of isostructural MOFs, known as M-CPO-27, which display coordinatively unsaturated metal sites (CUSs) when fully activated (guest solvent molecules both coordinated and uncoordinated to the metal atom are removed). Two of these frameworks (Ni and Co CPO-27) displayed exceptional performance over the entire cycle of activation, storage and delivery showing the largest storage and release of NO of any known porous material (up to 7 mmolg⁻¹). These frameworks would therefore be considered for initial research into the formulation of MOFs, for possible use in medical applications. It was shown that they still release large amounts of NO even when placed inside porous paper bags, creams or hydrocolloids. The other versions of M-CPO-27 also displayed significant adsorption of NO however they show poor total NO release. It was also shown that it is possible to synthesise both Ni and Co CPO-27 using microwave synthesis without any detrimental effect to the porous structure. Several iron-based MOFs were also investigated for NO storage and release. The results showed that Fe MIL-88 based structures adsorb good amounts of NO but only release a small amount of the irreversibly adsorbed NO. Two successfully amine grafted giant pore MOFs were then investigated to attempt to improve the NO adsorption and release. This result was not observed however, due to the poor total amine grafting coverage and pore blockage resulting from the amines. In-situ IR studies reveal that when exposed to NO, activated Fe MIL-100 forms a chemical bond with the NO. The studies also displayed that when water is then allowed to attempt to replace the NO that only a small amount of NO is actually released, the majority of the NO either remains chemically bonded to the Fe atom or forms N₂O in conjunction with a Fe-OH group. Other MOFs were also successfully synthesised and characterised for NO storage and release. Both Ni succinate and Ni STA-12 display good adsorption and excellent release of NO. This indicates that Ni based MOFs show the best results for NO adsorption and release. In the conclusion of the thesis I am able to categorise the NO release ability of MOFs based on composition and formulate a theory as to why this happens.

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13

Cuthbertson, B. H. "Nitric oxide in the lung". Thesis, University of Aberdeen, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.592302.

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Aim: To study the role of NO in inflammatory and immune processes within the lung. Methods: 1. A study of the in-vitro response of human neutrophils and whole blood cultures to exogenous NO and superoxide donors with regard to interleukin-8 and elastase accumulation. 2. In a randomised controlled study of inhaled NO versus control in ALI the effects of inhaled NO on inflammatory and immune responses within the lung was studied. Results: 1. NO donors are seen to have varying effects on interleukin-8 accumulation from human neutrophils and on interleukin-8 and elastase accumulation from whole blood incubation. 2. Inhaled NO therapy is seen to reduce time to resolution of ALI but did not effect mortality. Leucocyte NOS activity was reduced in the inhaled NO group whilst plasma total nitrite and nitrate was seen to increase. Bronchoalveolar (BAL) fluid leukotriene levels at 72 hours were also demonstrated to increase with inhaled NO treatment. BAL fluid myeloperoxidase was demonstrated to be a outcome marker in ALI. There was no difference between BAL fluid IL-8, elastase and myeloperoxidase levels between groups. Discussion: These results demonstrate that NO has significant effects on neutrophil function in-vitro. Inhaled NO therapy also reduces time to resolution of ALI which may reduce morbidity and cost of ITU care. Although there was an increase in BAL leukotriene levels in the treatment group there was not a significant rise in other inflammatory markers suggesting that inhaled NO may not be causing a large alteration in inflammatory response within the lung in ALI. The regulation of NOS activity may explain the mechanism of rebound phenomena upon inhaled NO withdrawal. Increased plasma total nitrite and nitrate demonstrates the importance of this route to metabolism on the biological breakdown of inhaled NO.

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14

Lam, Amanda Ay Jia. "Tetrahydrobioterin and nitric oxide metabolism". Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407919.

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15

Rhodes, Peter. "Indices of nitric oxide production". Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307982.

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16

Versnel, Jennifer Mary. "A nitric oxide holographic sensor". Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708672.

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17

McBride, Alan George. "Nitric oxide and oxygen metabolism". Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624510.

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18

Lozeille, JeroÌ‚me Andre. "Spectroscopy of nitric oxide complexes". Thesis, University of Sussex, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247957.

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19

Nguyen, Yen Hoang Le Dervan Peter B. Gray Harry B. "Wiring inducible nitric oxide synthase /". Diss., Pasadena, Calif. : California Institute of Technology, 2007. http://resolver.caltech.edu/CaltechETD:etd-09262006-134259.

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20

Greig, Iain Robert. "New nitric oxide donor drugs". Thesis, University of St Andrews, 1997. http://hdl.handle.net/10023/14105.

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Nitric oxide is a recognised dilator of vascular smooth muscle and therefore is central in the control of blood flow. A lack of blood flow in humans can have very important implications in a number of disorders of both cutaneous tissue and internal circulation. In this thesis we look at the synthesis of new nitric oxide donors, their stabilities and their possible medicinal usage. These donors have been based on the S-nitrosothiol group, connected to sugar moieties, simple amino acids or linked glycoaminoacids. The donors prepared have been used to investigate the skin blood flow and localised responses to nitric oxide, proving that NO has an important role in the maintenance of healthy skin. These will be further investigated as possible treatments for disorders involving a lack of cutaneous blood flow, such as connective tissue disorders and the repeated ulceration often seen in diabetic patients. A set of clinical trials have been carried out comparing the responses of healthy patients and sufferers of Raynaud's Phenomenon to exogenous nitric oxide. In this we have highlighted a number of differences and have helped to determine a possible cause of the disorder. We have prepared a number of slow release NO donors which have been shown to produce a sustained vasodilatory response in blood vessels with removed or damaged endothelial cells. These show promise for use in the treatment of patients with circulatory disorders, especially for subjects following treatment for atherosclerosis. Basic studies investigating the stabilities of these compounds have been carried out, in order to aid our understanding of their mode of breakdown.

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21

Isbell, T. Scott. "Nitrite conversion to nitric oxide biological mechaisms and therapeutic implications /". Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/isbell.pdf.

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22

Åkesson, Björn. "Islet constitutive nitric oxide synthase and nitric oxide production modulatory effects on insulin and glucagon secretion /". Diss., Lund, Sweden : Dept. of Pharmacology, University of Lund, 1998. http://catalog.hathitrust.org/api/volumes/oclc/41383563.html.

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23

Levy, Dan. "Local nitric oxide synthase expression and nitric oxide action in an animal model of neuropathic pain". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0034/NQ38484.pdf.

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24

Duarte, Américo José Gonzalez. "Characterization of Nitric Oxide Reductase (NOR) from pseudomonas nautica, a study on biologic nitric oxide reduction". Doctoral thesis, Faculdade de Ciências e Tecnologia, 2011. http://hdl.handle.net/10362/6680.

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Dissertation submitted to obtain the phD degree in Biochemistry, specialty in Physical- Biochemistry, by the Faculdade de Ciências e Tecnologia from the Universidade Nova de Lisboa
Denitrification is a metabolic pathway from the nitrogen cycle where nitrate is reduced to dinitrogen. This pathway involves four reduction steps: the nitrate reduction to nitrite, followed by the reduction to nitric oxide (NO), from this to nitrous oxide (N2O), and finally to dinitrogen. The enzymes involved in the mentioned steps are the nitrate reductases, the nitrite reductases, the nitric oxide reductases (NOR) and the nitrous oxide reductases, respectively. The NORs perform the NO reduction to N2O, using two substrate molecules, two protons and two electrons with the consequent product formation and water. These enzymes belong to the heme copper oxidase superfamily, since they are integral membrane proteins, with 12 transmembrane α-helixes and a set of conserved residues. They are composed by two subunits. The NorC subunit with a molecular weight of 17 kDa, comprises a low-spin heme c covalently bound to the polypeptide chain, with a His/Met coordination. The second subunit, NorB, also named the catalytic subunit, with a molecular weight of 56 kDa, harbouring two b-type hemes, one low-spin bis-His coordinated (heme b), a high-spin heme b (heme b3), His coordinated and a non-heme FeB. These last two iron centers are antiferromagnetic coupled and bridged by a μ- oxo/hydroxo group, and together they compose the catalytic diiron center. Recently Mössbauer spectroscopy proved that the catalytic heme b3 is in fact low-spin in both ferric and ferrous states, indicating a six-coordination environment for this iron center in both redox states. The Pseudomonas (Ps.) aeruginosa NOR crystal structure shows the presence of the His ligand simultaneously with the μ-oxo bridge in the as-isolated form. The substrate reduction mechanism is an issue of intense discussion, with the cis and trans-mechanisms taken in consideration. The cis-mechanism descries that NO reduction occurs in the catalytic center and only one of the iron atoms is coordinating the substrate during catalysis. The trans-mechanism describes NO reduction with the binding of one substrate molecule to each one of the iron atoms of the catalytic center. Different isolated NORs have the ability of reducing O2 to H2O in a four electrons/four protons reaction. The mechanism for O2 reduction is unknown, but it is presumed that substrate binds to the catalytic heme b3, analogous to the terminal oxidases. The main objective of this work was to isolate and characterize the Ps. nautica NOR, using different biochemical, and spectroscopic techniques.
Fundação para a Ciência e Tecnologia - bolsa de doutoramento (SFRH/BD/39009/2007)

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25

Schmachtenberg, Oliver. "Nitric oxide in the olfactory epithelium". [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=962820598.

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26

Klassen, Shaun Scott. "Nitric oxide-induced cardiomyocyte cell death". Thesis, University of British Columbia, 2006. http://hdl.handle.net/2429/31539.

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Nitric oxide (NO), a regulator of diverse cardiovascular functions, modifies cardiac cell viability through mechanisms that remain uncertain. Several pathways were studied to understand these effects. The possibility that the protein p53 is involved in the cardiomyocyte response to the NO donor s-nitrosoglutathione (GSNO) or the peroxynitrite donor 3- morpholinosydnonimine (SIN-1) was explored. These donors induced a concentration-dependent increase of cell death in cultured embryonic chick cardiomyocytes. Expression of p53 protein was increased in response to GSNO, specifically in the nucleus. GSNO also caused DNA damage, but pifithrin, an inhibitor of p53 transactivation activity, did not alter the extent of this damage or cell death. Therefore, the role of increased nuclear p53 in response to NO and NO-induced DNA damage may not be specifically operative in NO-induced cell death. The action of GSNO also appears independent of mitochondrial pathways in cell death, as there was no association of p53 with the mitochondria. Neither GSNO- or SIN-1-induced cell death was altered by cyclosporin A, suggesting that permeability transition pore opening is not operative in these modes of induction of death. In contrast to SIN-1, GSNO did not reduce mitochondrial transmembrane potential, implying separate mechanisms of cell death. Immunocytochemistry demonstrated increased amounts of nitrotyrosine in response to GSNO or SIN-1, confirmed by Western blot following SIN-1. FeTPPS, an isomerase that converts peroxynitrite into the less toxic nitrate, produced a significant reduction of SIN-1-induced cell death and cellular protein nitration. FeTPPS did not reduce cell death from GSNO alone, but did from the combination of GSNO and hydrogen peroxide, a condition which promotes the generation of peroxynitrite. In summary, NO-induced cardiomyocyte cell death is due in part to the disruption of normal cellular functions by nitration of key proteins. Peroxynitrite decomposition reduces protein nitration and cell death, while p53 appears functions independent of the mitochondria or gene transactivation and may act in other pathways, such as cell repair.
Medicine, Faculty of
Medicine, Department of
Experimental Medicine, Division of
Graduate

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27

Roy, Brijesh. "Regulation of the nitric oxide receptor". Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1445910/.

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The guanylyl cyclase-coupled nitric oxide receptor (GC) acts like a classical neurotransmitter receptor, binding the ligand NO and forming the second messenger cGMP. This thesis investigated the regulation of the NO receptor by endogenous regulators and two groups of pharmacological activators. Haem-mimetic compounds activate the NO-insensitive, haem-free form of the receptor. BAY58-2667 activated the haem-free receptor with half the efficacy of NO activating the haem-reduced receptor. These findings prompt reassessment of physiological and pathophysiological roles of the haem-free receptor, and contradict reports that haem mimetics also activate the haem-oxidised receptor. The second group of compounds activates GC by inhibiting receptor deactivation. BAY41-2272 activated purified GC with EC50= 43 23 nM in the presence of maximally stimulating NO concentrations, and this activation was prevented by NO scavengers. BAY41-2272 renders GC the most potent known NO detector (EC50 = 47 3 pM), confirming earlier theoretical predictions (Garthwaite, 2005). Recently a dual-site model for NO-stimulation of GC was proposed (Cary et al., 2005). Predictions of the Cary model were tested on rat cerebellar cells and platelets, using a new technique for delivering repetitive pulses of NO. The findings suggest that the proposed model is of doubtful relevance, and support the existing one site, two states model. The simple model is further refined by incorporation of regulation by nucleotides and Ca2+. In this new model both ATP and substrate GTP act as allosteric regulators. Inhibition by Ca2+ proved rather complex, involving two inhibitory sites that predominately affected NO-stimulated GC activity and also inhibited receptor deactivation. The new model also partially reconciles the different behaviour of GC when purified from its cellular environment. While this new model appears kinetically robust, further investigation is required to properly incorporate Ca2+ into the scheme and also to link these regulatory changes to the underlying structural modifications.

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28

Julyan-Gudgeon, John Howard Ross. "Nitric oxide and form-deprivation myopia". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0019/MQ48005.pdf.

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29

Gribbe, Örjan. "Experimental skin flaps and nitric oxide /". Stockholm, 2006. http://diss.kib.ki.se/2006/91-7357-043-5/.

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30

Ljung, Tryggve. "Nitric oxide in inflammatory bowel disease /". Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-602-2/.

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31

Schön, Thomas. "Nitric oxide in tuberculosis and leprosy /". Linköping, 2002. http://www.bibl.liu.se/liupubl/disp/disp2002/med749s.pdf.

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32

Sandström, Per A. "Nitric oxide, arginine and acute pancreatitis /". Linköping : Univ, 2004. http://www.bibl.liu.se/liupubl/disp/disp2004/med866s.pdf.

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33

Hambræus, Jonzon Kristina. "Hypoxic pulmonary vasoconstriction and nitric oxide /". Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4266-8/.

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34

Mancini, Lucia. "Nitric oxide regulation of bone metabolism". Thesis, Queen Mary, University of London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343902.

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35

Kharitonov, Sergei Alexandrovich. "Exhaled nitric oxide in airway diseases". Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266411.

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36

Hopper, Rachel Anne. "Nitric oxide and hippocampal synaptic plasticity". Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1444742/.

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Abstract (sommario):

Nitric oxide (NO) functions widely as a signalling molecule in the brain and has been implicated in several types of synaptic plasticity, including NMDA receptor-dependent long-term potentiation (LTP) in the hippocampus. The precise role played by NO in this and related phenomena is uncertain and the aim of my research was to explore this question. The principal receptor for NO possesses guanylyl cyclase activity, so that NO binding results in cGMP formation. NO has also been claimed to modify thiol residues (S'-nitrosation) and, through this mechanism, exert a negative feedback on NMDA receptors. Tests of this hypothesis were conducted by recording NMDA receptor-mediated field excitatory postsynaptic potentials in the CA1 region of rat hippocampal slices. Neither manipulation of endogenous NO levels nor application of exogenous NO had any effect. The reported inhibition of synaptic NMDA receptor function when NO is released by UV light from a caged derivative was confirmed, but a similar result was obtained using a combination of exogenous NO and UV light, casting doubt on the physiological relevance this effect. There has been debate over the isoform of NO synthase (endothelial, neuronal, or both) needed for hippocampal LTP and it has been suggested that LTP requires not only a phasic NO signal associated with tetanic stimulation but also a tonic level of NO. cGMP measurements in hippocampal slices indicated that endothelial NO synthase was largely responsible for the basal NO tone, and that T-type voltage-gated calcium channels may elicit the steady output of NO, presumably from endothelial cells. Electrophysiological tests conducted in CA1 found a deficit in LTP both in eNOS-deficient mice and in wild type mice subjected to selective nNOS inhibition. The results indicate that both isoforms of NO synthase participate in LTP but may perform distinct roles.

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37

Fairley, Brian. "Porphyrin models for nitric oxide synthase". Thesis, Heriot-Watt University, 2001. http://hdl.handle.net/10399/534.

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38

Pluciennick, Cecile. "Biomimetic models for nitric oxide synthase". Thesis, Heriot-Watt University, 2002. http://hdl.handle.net/10399/439.

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39

Feng, Gui-jie. "Regulation of inducible nitric oxide synthase". Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360104.

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40

Sadler, Claire Judith Anne. "Hypothalamic nitric oxide in weight regulation". Thesis, University of Liverpool, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.400387.

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41

Lewis, Randy Stewart. "Nitric oxide kinetics in biological systems". Thesis, Massachusetts Institute of Technology, 1995. http://hdl.handle.net/1721.1/36947.

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42

Hall, Catherine Naledi. "Nitric oxide inactivation in the brain". Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1445564/.

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Abstract (sommario):

Nitric oxide (NO) is a signalling molecule in the central nervous system and other tissues. NO synthesis and its immediate targets are well-characterised moleculaiiy, but little is known about how the NO signal is terminated. Recent work has suggested the existence of a biological sink for NO in dispersed brain tissue. This study aimed to discover the kinetic properties of NO inactivation in brain and to elucidate the mechanism(s) underlying this process. Measurements of cGMP accumulation in brain slices from cerebellum indicated that intact brain inactivates NO. When analysed using a model of NO diffusion and inactivation, the experimental data were consistent with the maximum rate of inactivation being fast (over 1 uM/s). It was inferred from the kinetics that biological inactivation of NO would predominantly affect NO signalling when several sources of NO are concurrently active. The mechanism of NO consumption initially studied in dispersed brain tissue has since been shown to be the reaction of NO with lipid peroxyls, a process that may have relevance to pathophysiology. Pharmacological and other tests showed that the breakdown of NO by cerebellar slices was, however, independent of this mechanism. Further manipulations also eliminated other potential routes of NO metabolism (reaction with red blood cells or superoxide, or autoxidation) as underlying causes. Lipid peroxide-independent NO inactivation was also found in acute and cultured cerebellar cells. The reaction exhibited marked oxygen- dependence. In dilute preparations, NO metabolism was largely lost on cell lysis, but was recoverable by addition of the electron donor NADPH. This activity resided in the membrane fraction following high speed centrifugation. Inactivation of NO in NADPH-treated lysates or membrane fractions, and in intact cells, was partially inhibited by cyanide. This evidence suggests the involvement of membrane-bound haem and flavoproteins. In concentrated tissue preparations and intact brain slices, however, an alternative process becomes dominant. Which of these mechanisms is most important physiologically requires further investigation. Their relative distributions with respect to the sites of NO release may be critical.

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43

Muizzi, Casanas Dayana Andreina. "Light Activated Nitric Oxide Releasing Materials". Bowling Green State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1435581276.

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44

Brady, Adrian J. B. "Nitric oxide and cardiac myocyte contraction". Thesis, University of Edinburgh, 1994. http://hdl.handle.net/1842/20215.

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Whether nitric oxide is implicated in the contractile function of isolated cardiac ventricular myocytes forms the major part of the work of this thesis. Contracting guinea-pig cardiac myocytes were studied in isolation in vitro using a videomicroscopy length detection system. Studies are presented which establish that nitric oxide attenuates contractility of cardiac ventricular myocytes, both when it is derived from exogenous sources, and when nitric oxide is released from adjacent endothelium in coculture with cardiac myocytes. The coronary microcirculation is in close proximity to cardiac myocytes within the myocardium, thus endothelium-derived nitric oxide may have an important tonic effect on myocardial contractility. This may be particularly important when the diffusing distance from endothelial cell to myocyte is altered in disease states. Myocardial contractility is impaired in endotoxic shock. The hypothesis that this is caused by production of nitric oxide within cardiac myocytes is examined. A model of endotoxic shock was developed. Contractility of cardiac myocytes was substantially impaired. Much of this impairment was caused by nitric oxide production within the cardiac myocytes themselves. Inhibition of nitric oxide synthesis in these cells restored contractility towards normal. Healthy myocytes did not produce effective amounts of nitric oxide. Induction of nitric oxide synthase activity within cardiac myocytes may account for much of the depressed contractility of endotoxic heart failure. Myocardial contractility is impaired following ischaemia-reperfusion. Experiments examining myocyte behaviour in this situation are discussed, but whether activation of nitric oxide synthase contributes to the impaired contractility of myocytes following ischaemia is not established.

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45

Hemmingsson, Tryggve. "Exhaled nitric oxide in extreme environments". Stockholm : Karolinska institutet, 2009. http://diss.kib.ki.se/2009/978-91-7409-609-5/.

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46

Sigrist, Nadja E. "Nitric oxide production in canine osteoarthritis /". [S.l.] : [s.n.], 1998. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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47

Wei, Xiao-qing. "Inducible nitric oxide synthase gene targeting". Thesis, University of Glasgow, 1995. http://theses.gla.ac.uk/8351/.

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Abstract (sommario):

Nitric oxide (NO) is a critical mediator of a variety of biological functions, including vascular and muscle relaxation, platelet aggregation, neuronal-cell function, microbicidal and tumoricidal activity, and a range of immunopathologies. NO is derived from L-arginine and molecular oxygen in a reaction catalysed by NO synthase (NOS). Three isoforms of NOS have been identified; neuronal constitutive NOS (ncNOS), endothelial constitutive NOS (ecNOS), and inducible NOS (iNOS). ncNOS and ecNOS are calcium-dependent, present constitutively in a variety of tissues and produce physiological concentrations of NO. However, large amounts NO are produced by iNOS which are expressed in cells such as macrophage after stimulation with a number of cytokines, including interferon-gamma (IFN-γ), tumour necrosis factor-alpha (TNF-α), and bacterial lipopolysaccharide (LPS). Findings of iNOS biological functions are based mainly on experiments using L-arginine analogues such as L-NG monomethyl arginine (L-NMMA) which competitively inhibits NO Synthase. These inhibitors are not NOS isoform selective and have differential bioavailability, and hence often render interpretation of results difficult. To directly define the iNOS biological functions, I constructed a strain of iNOS gene targeted mice. The first step of a gene targeting experiment is typically cDNA cloning and sequencing. A cDNA library was constructed in the vector λ ZAPII using mRNA isolated from J774 macrophages activated with IFN-? and LPS. Six independent positive colonies were found in the screen with both 5' and 3' specific probes and were subcloned in pBluescript. A full-length iNOS cDNA was constructed using the clones isolated from the library. Double strand cDNA sequence analysis showed that the J774 iNOS clone was identical to that of the Raw 264.7 macrophages iNOS cDNA sequence. A replacement-type targeting construct was prepared from 129/sv genomic DNA. A single targeted clone was identified amongst 636 screened after two independent electroporations of the CGR8 embryonic stem cell line. Gene replacement was detected by both 5' and 3' specific external probes. Five of ten chimeras generated gave germ line transmission. No homozygous mice were found by Southern blot analysis with 5' and 3' external probe in the offspring from heterozygous mice (FI) breedings. The iNOS gene had been altered by replacement with gene targeting construct and 5' iNOS gene translocation which could be detected by internal probe Southern blot analysis. Using the internal probe, mutant homozygous, heterozygous and wild-type mice were found in the offspring from heterozygous breedings. The ratio of these three genotypes was 21:47:25. Northern blot analysis with 5' iNOS cDNA probe showed that a large messenger appeared in the macrophages of homozygous mice when the cells were activated with IFN-γ and LPS in vitro. However there was no detectable iNOS protein translation by western blot analysis using monoclonal or polyclonal anti-iNOS antibodies.

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48

Thorman, Rachel E. "Nitric oxide emissions from agricultural soils". Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/27539.

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Nitric oxide (NO) plays a crucial role in photochemistry, particularly in the formation of tropospheric ozone. In soil the biogenic production of NO is primarily conducted by the microbial processes of nitrification and denitrification. The management of soils may, therefore, significantly impact on local atmospheric NO concentrations. The aim of this study was to investigate the influence of various agricultural practices on the magnitude of NO flux, specifically the role of tillage technique in an arable system and the comparative effect of organic wastes and inorganic fertilisers applied to a grassland system. Fluxes of NO from a sandy loam/silty clay loam soil cropped with spring barley, with and without the addition of NH4NO3 fertiliser (80 kg N ha'1), were measured using a static chamber method. The site was managed to compare the influence of 3 tillage regimes; conventional mouldboard ploughing, deep ploughing and direct drilling. There was a marked effect on the magnitude of NO fluxes fromboth the nitrogen and tillage treatment. Nitric oxide fluxes ranged between2-1deposition and emission from -2.6-49.5 jug NO-N m" h" (fertilised & ploughed) and -2.0-2.0 /xg NO-N m2 h"1 (unfertilised & direct drilled). Emissions of NO were significantly larger from the ploughed soils than from the direct drilled soils, primarily due to the increased water filled pore space stimulating denitrification and reducing NO emission. Of the fertiliser N added 0.002-0.011% was lost as NO. The flux of NO between ungrazed grassland (clay loam) and the atmosphere was measured following the application, at a target rate of 120 kg available N ha"1, of either cattle slurry, anaerobically digested sewage sludge, thermally dried sewage sludge pellets, mineral NPK fertiliser & Ficote 70? slow release fertiliser or no fertiliser addition. Nitric oxide emissions were stimulated by both organic wastes and NPK inorganic fertiliser, with cumulative fluxes markedly higher from the organic wastes, particularly from the sewage sludge pellets, which were 1.3-42.3 times larger than the other treatments. It was estimated that 0.0004-0.03% of the applied total N was released as NO. Complementary laboratory studies designed to investigate the influence of dominant environmental factors on NO emission from repacked soil cores under controlled conditions showed that NO emission was 2.2-23.5 times larger from soil amended with sewage sludge pellets. The magnitude of the flux was associated with a soil saprophytic fungus and incorporation of the pellets appeared to reduce the cumulative NO loss. In field and laboratory studies NO flux rate was strongly dependent on soil NH4+-N, soil NO3VN, soil water filled pore space and the pattern of precipitation, particularly around fertiliser application. The data suggest that NO was primarily produced by nitrification in the grassland soil and a combination of both denitrification and nitrification in the arable soil. The total flux from UK agricultural land was estimated as 0.007 Tg of NO-N. This is approximately 1.5% of the annual UK total NO-N production. Based on the evidence collected from the 2 field studies, therefore, the emission of NO from agricultural soils in the UK is not significant in terms of its contribution to the NO-N total. Flowever, agricultural soils may emit NO to the atmosphere and produce localised concentrations high enough (e.g. after fertiliser application) to generate harmful levels of tropospheric O3.

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49

Cheng, Wendy Ho Yee. "Nitric oxide and nitric oxide donors : modulation of mitochondrial function and effects of myocardial ischaemia-reperfusion injury". Thesis, University of Bristol, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.560497.

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Abstract (sommario):

Nitric oxide (NO) may modulate mitochondrial O2 consumption in the heart, and provide another level of respiratory control under normal or hypoxic conditions. NO and NO donors have also been proposed to have both beneficial and deleterious effects during ischaemia-reperfusion (IR) injury, and both of these maybe mediated by interactions of NO with mitochondria. The aims of the research in this thesis were to investigate (i) whether there is a specific form of mitochondrial nitric oxide synthase (NOS), (ii) which NO donors release NO spontaneously and which require bioactivation, (iii) whether different NO donors are protective or deleterious during IR injury, (iv) the effect of NO donors on mitochondrial membrane permeability transition pore (mPTP) opening. In this study, using 3 different techniques (Western blotting, immunoprecipitation and DAF fluorescence), no evidence was found to suggest the existence mitochondrial NOS in highly purified heart and liver mitochondria. However, it was possible to detect all forms of NOS in crude heart and liver mitochondria, and the same applied for the ryanodine receptor and caveolin, in "mitochondrial" fractions. Despite the fact that NO donors are commonly used in medicine and in research, in many cases it is still unclear as to how NO is released from the NO donors; whether it is spontaneously released or whether bioactivation is required. Using the NO- sensitive fluorescent dyes DAF-2 and DAF-2 DA, the results of this study showed that the NO donors DEA and SIN-l spontaneously released NO. SNAP, a donor that has been assumed to be spontaneous, showed no release of NO. Sodium nitroprusside did show significant spontaneous release of NO, but only at 5 and 10 mM. The novel NO donor NCX2057 was the only NO donor that showed release of NO by mitochondrial metabolism. The nitrates BDMN and ISMN both released NO in post-mitochondrial supernatant, indicating the involvement of cytosolic enzymes in NO donor metabolism. Previous studies have shown that NO can have both protective and deleterious effects in whole heart IR injury. In this study it was shown that the administration of the NO donors, SNAP and DEA before the onset of global ischaemia and throughout reperfusion, resulted in a concentration-dependent protection against IR injury. Beyond a concentration threshold level (40 ~ SNAP and 2 ~ DEA), the protection was lost. Since IR injury is critically regulated by the opening and closing of the mPTP during reperfusion, the effects of DEA on mPTP opening, mitochondrial Ca2+ uptake and membrane potential were investigated using isolated mitochondria. The lower concentrations of DEA (2-25 flM) caused partial mitochondrial membrane depolarisation, sensitised the mPTP to Ca2+ and promoted mPTP opening. By contrast, the higher concentrations of DEA depolarised the mitochondrial membrane potential, prevented Ca2+ uptake and inhibited mPTP opening. This biphasic effect observed could be attributed to the inhibition of cytochrome c oxidase, as potassium cyanide had similar effects on membrane potential, Ca2+ uptake and mPTP opening as DEA. DEA also inhibited mPTP opening under de-energised conditions, indicating that in addition to modulating mPTP opening via inhibition of cytochrome c oxidase, DEA can also directly interact and modify mPTP components, possibly via nitration.

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50

Lahiri, Mayurika. "Characterisation of nitric oxide synthase isoforms and nitric oxide synthase activity in human breast cancer cell lines". Thesis, University of Wolverhampton, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391489.

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Tesi sul tema "Nitric oxide"

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